基于高效液相色谱-加热电子喷雾离子化-高分辨质谱和细胞代谢组学的广藿香非挥发性成分抗炎机理研究。

Jing Wenguang, Lin Xiaoyu, L I Chu, Zhao Xiaoliang, Cheng Xianlong, Wang Penglong, Wei Feng, M A Shuangcheng
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引用次数: 0

摘要

目的:探讨广藿香中的非挥发性成分的抗炎成分及其作用机制:方法:采用高效液相色谱-加热电子喷雾离子化-高分辨质谱(HPLC-HESI-HRMS)分析广藿香非挥发性成分的化学成分。利用脂多糖(LPS)诱导的 RAW264.7 细胞炎症模型评价了藿香正气水成分的抗炎活性,并利用细胞代谢组学的多元统计分析研究了藿香正气水成分的抗炎机制:结果:采用 HPLC-HESI-HRMS 对广藿香的非挥发性成分进行了表征,鉴定出 36 种黄酮类化合物和 18 种其他成分。藿香正气水中的这些成分不仅对LPS诱导的RAW264.7细胞炎症模型有良好的保护作用,还能通过下调精氨酸代谢、氨基酰-tRNA生物合成、多元醇/山梨醇途径,调节精氨酸、L-亮氨酸、胆固醇、果糖和山梨醇的表达水平,从而减轻炎症反应,减少细胞损伤:结论:藿香正气水中的非挥发性成分具有良好的抗炎作用,通过调节内源性代谢途径来减轻炎症反应,从而发挥治疗作用。
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Anti-inflammatory mechanism of the non-volatile ingredients originated from Guanghuoxiang () based on high performance liquid chromatography-heated electron spray ionization-high resolution mass spectroscope and cell metabolomics.

Objective: To explore the anti-inflammatory components and mechanism of the non-volatile ingredients of patchouli.

Methods: High performance liquid chromatography-heated electron spray ionization-high resolution mass spectroscope (HPLC-HESI-HRMS) was used to analyze the chemical constituents of the non-volatile ingredients of patchouli. The anti-inflammatory activity of ingredients was evaluated using lipopolysaccharide (LPS) induced RAW264.7 cell inflammation model, and the anti-inflammatory mechanism was investigated using multivariate statistical analysis of cell metabolomics.

Results: The non-volatile ingredients of patchouli were characterized by HPLC-HESI-HRMS, and 36 flavonoids and 18 other components were identified. These ingredients of patchouli not only had a good protective effect on the LPS-induced inflammation model of RAW264.7 cells, but also regulated the expression levels of arginine, L-leucine, cholesterol, fructose and sorbitol by down-regulating arginine metabolism, aminoacyl-tRNA biosynthesis, polyol/sorbitol pathway, so as to reduce inflammation and reduce cell damage.

Conclusion: The non-volatile ingredients of patchouli had good anti-inflammatory effect and exerted its curative effect by regulating endogenous metabolic pathway to reduce inflammatory response.

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